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Brain Res Bull. 2002 Jun;58(2):149-60.

Withdrawal from dependence upon butorphanol uniquely increases kappa(1)-opioid receptor binding in the rat brain.

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1
Department of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson, MS 39216, USA.

Abstract

Changes in kappa(1)-opioid receptor binding have been implicated in the development of dependence upon and withdrawal from butorphanol. Autoradiographic characterization of binding for brain kappa(1)-([3H]CI-977), mu-([3H]DAMGO), and delta-([3H]DPDPE) opioid receptors was performed in rats undergoing naloxone-precipitated withdrawal from dependence upon butorphanol or morphine. Dependence was induced by a 72h i.c.v. infusion with either butorphanol or morphine (26nmol/microl/h). Withdrawal was subsequently precipitated by i.c.v. challenge with naloxone (48 nmol/5 microl/rat), administered 2h following cessation of butorphanol or morphine infusion. During withdrawal from butorphanol, but not morphine, kappa(1)-opioid receptor binding was increased significantly in the frontal cortex, posterior basolateral amygdaloid nucleus, dorsomedial hypothalamus, hippocampus, posterior paraventricular thalamic nucleus, ventral tegmental area and locus coeruleus. In contrast, mu-opioid receptor binding decreased in these brain regions in naloxone-precipitated withdrawal from morphine, but not butorphanol, while binding for delta-opioid receptors was altered in both withdrawal groups. The brain kappa(1)-opioid receptor appears to be more directly involved in the development of physical dependence upon, and the expression of withdrawal from, butorphanol, as opposed to the prototypical opioid analgesic, morphine.

PMID:
12127012
[Indexed for MEDLINE]

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